Disease relevance of Amhr2

• A subclone of rat pituitary tumor cells, designated GH3/C14, was isolated from the parent population of GH3 pituitary cells and was estrogen-dependent for growth in vivo [1].
• We have recently identified a pathogenic epitope, clone 14 (C14), responsible for formation and deposition of glomerular immune complexes that is contained within the small subunit of the Heymann nephritis antigenic complex (HNAC) [2].
• Here we report the cloning and expression of C14-derived single chain TCR (scTCR) molecules in an Escherichia coli expression system [3].
• We have characterized the mouse thymoma/rat V beta 8.2+ T-cell hybridoma C14/BW12-12A1 by fluorescence-activated cell sorting analysis and have used immunoaffinity chromatography to purify class I molecules from these cells [4].
• Using a calibration of the fluorescence signal with fatty acids in the C14 to C20 chain-length range, fatty acid consumption by Pseudomonas fragi and rat liver microsomal acyl-CoA synthetase activities are measured down to 0.05 microM/min with a data sampling rate of 10 points per second [5].

High impact information on Amhr2

• In some regions localizations of Ins(1,4,5)P3 receptors resemble those of protein kinase C14, while in others they differ markedly, suggesting a novel mechanism whereby the relative activity of the two limbs of the PI cycle can be differently regulated [6].
• Further examination of rat pituitary cell line GH3/C14 showed that at least the physiologic concentration of L-thyroxine was required for estrogen-dependent growth in vivo [7].
• Tumor formation by GH3/C14 cells inoculated into male animals was not supported by either exogenous progesterone or hydrocortisone acetate [1].
• Administration of BSP or probenecid simultaneously with [C14] penicillin resulted in increased plasma retention and reduced kidney and urinary bladder content of [14C] penicillin and a correlation coefficient of -0.8 between total kidney/plasma radioactivity and percent of protein-bound radioactivity bound to ligandin in the kidney [8].
• The MIS type II receptor (MISRII), which provides specificity for MIS, is also expressed in the adult testis, ovary, and uterus [9].

Biological context of Amhr2

• Comparison of the linkage map with corresponding regions of the published rat genome sequence revealed several candidate genes for the mp mutation, including the Dhh, Tegt, Gdp3, and Amhr2 genes [10].
• The encephalitogenic rat T cell clone C14 recognizes the myelin basic protein 69-89 peptide in the context of the RT1B major histocompatibility complex (MHC) class II molecule [3].
• In the immature rat testis, there is a marked developmental increase in AMH type II receptor (AMHRII) messenger RNA (mRNA) expression in Sertoli cells, concomitant with the initiation of spermatogenesis [11].
• ADRP was modified, apparently post-translationally, and one modification apparently was acylation, primarily with C14, C16 and C18 fatty acids [12].
• Medium chain length (C8-C12) fatty acids were predominantly recovered in the free fatty acid fraction, whereas the remaining tri- and diglycerides became richer in long chain (greater than or equal to C14) fatty acids suggesting a preferential lipolysis of medium chain fatty acid ester bonds [13].

Anatomical context of Amhr2

• The MIS type II receptor (MISRII)-expressing cells are initially present in the coelomic epithelium of both male and female urogenital ridges, and then migrate into the mesenchyme surrounding the male Müllerian duct under the influence of MIS [14].
• Alk2-specific small interfering RNA (siRNA) blocks both the transition of MISRII expression from the coelomic epithelium to the mesenchyme and Müllerian duct regression in organ culture [14].
• Marked C14 mRNA expression was also detected in the female gonads [15].
• Northern analysis revealed that the MIS type II receptor messenger RNA is highly expressed in embryonic, pubertal, and adult testes and ovaries, as well as in the gravid uterus [16].
• Thioesterase II is capable of shifting the product specificity of rat mammary gland fatty acid synthetase from predominately long chain fatty acids (C14, C16, and C18) to mainly medium chain fatty acids (C8, C10, and C12) [17].

Associations of Amhr2 with chemical compounds

• The domain structure of the C14-encoded protein corresponds with the structure of the other known transmembrane serine/threonine kinase receptors [15].
• GH3/C14 cells inoculated into host animals formed tumors in intact females, estrogen-treated ovariectomized females, and estrogen-treated males, but not in untreated intact or castrated males, or untreated ovariectomized females [1].
• The inducers are saturated fatty acids of two groups: butyric acid and acids with chain lengths from C13 to C16, especially myristic acid (C14) [18].
• In addition, antibodies eluted from glomeruli of HN rats and antibodies to a C14 fusion protein immunoprecipitated gp330 and the 44-kDa protein, demonstrating that the epitopes responsible for the initial events of HN are accessible within the complex [19].
• Nitrosomethylalkylamines with chain lengths from C4 (n-butyl-) to C14 (n-tetradecyl-) were each administered in three rats at doses equimolar with 12 mg of the butyl compound [20].

Other interactions of Amhr2

• Anti-müllerian hormone and anti-müllerian hormone type II receptor messenger ribonucleic acid expression during postnatal testis development and in the adult testis of the rat [11].

Analytical, diagnostic and therapeutic context of Amhr2

• C14 scTCR was able to bind soluble rat MHC class II molecules bearing covalently coupled Gp-BP-(69-89) peptide, as analyzed using surface plasmon resonance [3].
• Judging from the C14-activity curves in ureter-ligated and nephrectomised rats a substantial glomerular filtration continued after obstruction of the urine flow [21].
• After a 14-day intravenous infusion, [C14] galactose and [C14] glycine absorption (pmol/cm2 intestine), mucosal DNA content (microg/mg mucosa), and protein content (microg/mg mucosa) were measured in the small intestine of each rat [22].
• When C14-labelled N-methyltryptamine was administered by intravenous injection to rabbits, C14-dimethyltryptamine was found in lung, the principle site of the methyltransferase that biosynthesizes this psychotogen [23].

References